Infectious Diseases

Infections of the oral cavity, neck, and head

OVERVIEW: What every practitioner needs to know

This is a broad subject area. The topics to be covered include odontogenic orofacial “space” infections; suppurative parotitis; peritonsillar abscess; and deep neck space infections, including submandibular (Ludwig’s angina), lateral pharyngeal, and retropharyngeal space infections. Although rare in the post-antibiotic era, deep space infections of the head and neck are potentially life-threatening. A clear understanding of their inter-relationships, anatomic routes of potential spread, and salient clinical presentations is critical to successful management and prevention of these infections.

Odontogenic orofacial infections arise either from dental caries or periodontal infections that have extended beyond the alveolar bone to involve the fascial spaces around the face and oral cavity. These infections tend to spread along planes of least resistance from the supporting structures of the affected tooth. In the maxilla, the alveolar bone is weakest on the buccal side throughout. In the mandible, the alveolar bone is weakest in the lingual aspect posteriorly affecting the molar teeth, and on the buccal side more anteriorly involving the incisors and canine teeth. Thus, location of the affected tooth predicts the route of spread and which orofacial spaces become infected (see
Figure 1).

Figure 1.

Routes of spread of odontogenic orofacial infections along planes of least resistance. A, coronal section in the region of the first molar tooth: a, maxillary antrum; b, nasal cavity; c, palatal plate; d, sublingual space (above the mylohyoid muscle); e, submandibular space (below the mylohyoid muscle); f, intraoral presentation with infection spreading through the buccal plates inside the attachment of the buccinator muscle; g, extraoral presentation to buccal space with infection spreading through the ubccal plates outside the attachment of the buccinator muscle. B, lingual aspect of the mandible: a, apices of the involved tooth above the myohyoid muscle, with spread of infection to the sublingual space; b, apices of involved tooth below the mylohyoid muscle, with spread of infection into the submandibular space.

The fascial spaces around the mouth and face, which are most commonly implicated in odontogenic infections, are shown in
Figure 2. Other non-odontogenic sources of infection include suppurative parotitis, peritonsillar abscess, sinusitis, and mastoiditis.

The main clinical presentation of various orofacial odontogenic infections are summarized in Table I. The location of these space infections can be helpful in identifying the underlying infected tooth and suggests the potential pathways for spread into deeper fascial space infections of the head and neck (see Figure 3).

Table I.

Orofacial space infections

Usual dental source

Clinical features

Pain

Trismus

Swelling

Dysphagia

Dyspnea

Masticator

Masseteric & pterygoid

Molars (especially 3rd)

+

+++

May not beevident (deep)

–

–

Temporal

Posterior maxillary molars

+

–

Face, orbit (late)

–

–

Buccal

Bicuspids, molars

±

±

Cheek (marked)

–

–

Canine

Maxillary canines, incisors

++

–

Upper lip, canine fossa

–

–

Infratemporal

Posterior maxillary molars

+

–

Face, orbit (late)

±

±

Submental

Mandibular incisors

++

–

Chin (firm)

–

–

Figure 3.

Potential pathways of spread into deep fascial space infections of the head and neck.

Epidemiology

Both dental caries and periodontal disease are common conditions. According to the National Health and Nutrition Examination Survey during1999-2004:

42% of children and adolescents and 90% of adults had dental caries in their primary teeth.

Prevalence of moderate to severe periodontal disease was 5% among those 35-49 years of age, 11% among 50-64 years of age, 14% among 65-74 years of age, and 20% among those older than 75 years of age.

Both are important causes of tooth loss after 65 years of age.

About 25% of all adults older than 60 years of age have lost all their teeth (edentulous), one-half from dental caries and one-half from severe periodontitis.

Dental caries are a more important cause of tooth loss before 35 years of age.

Periodontal disease is more important after 35 years of age.

The prevalence of orofacial space infections as a complication of dental caries or periodontal disease is unknown.

Predisposing factors

Poor oral hygiene

Advancing age

Tobacco use

Sugar-rich diet (dental caries)

Hormonal effects, such as puberty, menstruation, and pregnancy (periodontal disease)

Imaging studies

CT of face and neck to assess source and extension of orofacial space infections ($$)

Indication for consultation

Dentistry – oral hygiene and dental extractions

Oral surgery – surgical drainage of orofacial space infections

Therapeutic considerations

Although surgical drainage of loculated pus and dental extraction are the mainstay of therapy, antibiotic treatment is required to halt local spread of infection and prevent hematogenous dissemination.

Anti-infective agents are generally indicated if fever and regional lymphadenopathy are present or when infection has perforated the bony cortex and spread into surrounding soft tissues. Severely immunocompromised patients are particularly at risk for rapidly spreading orofacial infections and bacteremia. Empiric antimicrobial therapy should be initiated promptly in such patients.

The choice of specific antimicrobial regimens for odontogenic orofacial infections is empirical based on anticipated causative pathogens and immune status of the host. This is because specimens obtained extraorally to avoid contamination by the oral commensal flora are rarely available. Odontogenic orofacial space infections are usually polymicrobial involving both strict anaerobes and facultative bacteria within unique ecosystems of the dental plaque and gingival crevice.

The most prevalent anaerobic bacteria include gram-positive cocci, such as Peptostreptococcus spp., and gram-negative rods, such as Bacteroides spp., Fusobacterium spp., Prevotella spp. and Porphyromonas spp. The most prevalent aerobes are facultative gram-positive cocci such as Streptococcus mutans, and viridans streptococci. Facultative gram-negative bacilli and S. aureus (including MRSA) are uncommon in immunocompetent hosts but may be more important in immunocompromised patients. The choice of initial antimicrobial regimens directed at these pathogens in the normal or immunocompromised hosts are shown in Table II.

Whereas the causative microorganisms in odontogenic orofacial space infections were universally susceptible to penicillin in the past, this is no longer the case. β-lactamase production among oral anaerobes is increasingly recognized, particularly among Fusobacterium spp. and pigmented Prevotella spp. Treatment failure with penicillin alone has been well documented. Thus, penicillin monotherapy is no longer recommended. Penicillin plus metronidazole or a β-lactam-β-lactamase inhibitor combination (e.g., ampicillin-sulbactam) is recommended. Clindamycin, doxycycline, or moxifloxacin is an alternative for penicillin-allergic patients. Erythromycin and tetracycline are not recommended because of their lack of optimal anaerobic activity and increasing resistance among some strains of streptococci.

In immunocompromised hosts, broad-spectrum coverage for facultative gram-negative bacilli should be included. Combination therapy with a third or fourth generation cephalosporin plus metronidazole, or monotherapy with piperacillin-tazobactam, or a carbapenem (imipenem or meropenem) is indicated. In addition, patients with risk factors for methicillin-resistant Staphylococcus aureus (MRSA) infection should be treated empirically with vancomycin (15-20 mg/kg IV q 12h) or linezolid (600 mg IV q 12h). Risk factors for MRSA include history of intravenous drug abuse, comorbid disease (e.g., diabetes mellitus), and residence in a community or hospital with substantial incidence of MRSA.

Other treatment modalities include:

Surgical incision and drainage of loculated space infection

Dental extraction and restorative treatment

Hyperbaric oxygen treatment of osteomyelitis of the jaw, if poor response to antibiotics alone

Pathogenesis

Both dental caries and periodontal disease are initiated by dental plaques composed of unique ecosystems of microorganisms embedded in a biofilm on the tooth surface

Plaque on the tooth surface above the gingival margin (supragingival plaque) consists of acidogenic (acid-producing) and aciduric (able to grow at low pH) bacteria, which cause dental caries and may invade the pulp (pulpitis or endodontic infection); infection eventually perforates the alveolar bony (periapical abscess) and spread into orofacial fascial spaces.

Plaque on the tooth surface below the gingival margin (subgingival plaque) consists of proteolytic and histotoxic bacteria, which cause periodontal infection (gingivitis, periodontitis, or periodontal abscess); such infections may eventually penetrate into the deeper fascial spaces of the face and mouth.

The local anatomic barriers of bone, muscle, and fascia predetermine the routes of spread, extent, and clinical manifestations of many orofacial infections of odontogenic origin.

If pus perforates through either the maxillary or mandibular buccal plate inside the attachment of the buccinator muscle, infection will be intraoral; if the perforation is outside this muscle attachment, infection will be extraoral (see Figure 1A). Thus, infection of the upper and lower molars, lower incisors, and lower canine teeth is often accompanied by extraoral manifestations.

When a mandibular infection perforates lingually, it presents in the sublingual space if the apices of the involved teeth lie above the attachment of the mylohyoid muscle (e.g., mandibular incisor, canines, premolars, and first molars) and in the submandibular space if below the attachment of the muscle (e.g., the second and third molars; see Figure 1B)

Buccal space infections – These arise primarily from mandibular or maxillary bicuspid or molar teeth, the apices of which lie outside of the buccinator muscle attachments. They are readily diagnosed because of marked cheek swelling but with minimal trismus or systemic symptoms (see Figure 4).

Canine space infections – These originate from the maxillary incisors and canines and manifest as dramatic swelling of the upper lip, canine fossa, and frequently the periorbital tissues (see
Figure 5). Pain is usually moderate, and systemic signs are minimal. Occasionally, direct extension of infection into the adjoining antrum leads to purulent maxillary sinusitis.

Submental space infections – These originate from a mandibular incisor that perforates below the mentalis muscle. The chin appears grossly swollen and is firm and erythematous.

Masticator space infections – These infections typically originate from the third molar tooth to involve the masticator spaces consisting of the masseteric, pterygoid, and temporal space components (see Figure 6). These spaces intercommunicate with each other, as well as the buccal and deeper peripharyngeal fascial spaces (see Figure 2). The clinical hallmark of infection is trismus with pain in the area of the body or ramus of the mandible (see Figure 7). Swelling may not be prominent since the infection is beneath large muscle masses. When present, swelling tends to be brawny and indurated, suggesting the possibility of cervicofacial actinomycosis or mandibular osteomyelitis.

Temporal space infections – These infections typically originate from the posterior maxillary molar teeth. Swelling may be limited to the preauricular region and an area over the zygomatic arch (see Figure 8). As infection progresses, the cheek, eyelids, and whole side of the face may be involved. Infection may extend directly into the orbit via the inferior orbital fissure and produce proptosis, optic neuritis, and abducens nerve palsy (see Figure 9).

Infratemporal space infections – An infratemporal space infection usually originates from the third maxillary molar tooth. Clinically, marked trismus and pain are present, but very little swelling is observed early in the course. Late manifestations are similar to those of temporal space infections, including extension into the orbit through the inferior orbital fissure. Infection may also extend internally to involve an area close to the lateral pharyngeal wall, resulting in dysphagia.

Figure 7.

Figure 8.

Temporal space infections. The temporal space is divided by the temporalis muscle into a superficial component enclosed by the masseter muscle and a deep component enclosed by the medial pterygoid muscle

Figure 9.

Deep temporal space infection with spread to the right parotid space and the orbit. This patient developed right optic neuritis with permanent loss of vision. A, frontal view; B, lateral view showing pre-auricular swelling.

Prevention

Rigorous brushing with fluoridated toothpaste and dental flossing after each meal

Dietary counseling to reduce sugar-rich foods or beverages

Modification of risk factors for dental caries such as tobacco smoking

Early detection and treatment of dental caries and advanced periodontitis

WHAT'S THE EVIDENCE for specific management and treatment recommendations?

Although an independent association between periodontal disease and atherosclerotic vascular disease is well recognized, a causal relationship has not been established. Even though periodontal interventions result in a reduction in systemic inflammation and endothelial dysfunction in short-term studies, no evidence exists that they prevent the development of atherosclerotic vascular disease or its outcomes in the long term.

Imaging studies

Ultrasound to detect frank abscess or stones within Stensen’s duct or parenchyma

CT to detect stones and differentiate suppurative cellulitis from abscess or solid tumor

MRI to detect extension of infection into the deep peripharyngeal structures

Indication for consultation

Intensive care for sepsis and hypotension

Respirology or Anesthesiology for impending airway obstruction

Oral Surgery for surgical drainage

Therapeutic considerations

Treatment includes hydration and intravenous antibiotics. Since suppurative parotitis may invade deep fascial spaces of the head and neck and is potentially life-threatening, outpatient management with oral antibiotics is not advised.

Initial empirical antimicrobial regimens are based on the expected microbiology and host factors, such as comorbid conditions and immunosuppression (see Table III). The microbiology is quite variable and often polymicrobial involving both aerobic and anaerobic bacteria. S. aureus (including MRSA) is the most frequent isolate (about one-third of patients) followed by viridans streptococci. Facultative gram-negative organisms, such as Enterobacteriaeae, H. influenzae, Eikenella corrodens, and other gram-negative bacilli, are often seen in hospitalized patients. Pigmented Prevotella and Porphyromonas spp., Fusobacterium spp., and Peptostreptococcus spp. are the most common anaerobes.

Oral step-down regimens

Step down therapy may be considered once the patient has improved and surgical management is deemed unnecessary. The choice of oral regimens for step-down therapy should ideally be guided by culture and susceptibility data.

Imaging studies

Imaging is not necessary to make the diagnosis of peritonsillar abscess but may be helpful in differentiating cellulitis from abscess and other deep neck space infections and to assess possible complications (e.g., airway compromise, extension to lateral pharyngeal space, etc.).

Indication for consultation

Therapeutic considerations

The first step is upper airway management to treat respiratory distress and prevent aspiration of abscess contents.

Needle aspiration should be attempted to decompress abscess and obtain pus for Gram stain, cultures, and susceptibility testing. This is performed in Trendelenburg position with topical anesthesia and under ultrasound guidance.

Trial of empirical antibiotic therapy before definitive surgery if no evidence of airway compromise, severe trismus, or other complications.

Oral step-down regimens

Step down therapy may be considered once the patient has improved and surgical management is deemed unnecessary. The choice of oral regimens for step-down therapy should be guided by culture and susceptibility data.

Surgical drainage by needle aspiration, incision and drainage, or tonsillectomy

Needle aspiration is better tolerated and the preferred procedure

“Quinsy tonsillectomy” – aspiration followed by tonsillectomy in single procedure is an option

Indications for interval tonsillectomy include:

Significant upper airway obstruction or other complications

Failure of abscess resolution despite other drainage procedures

Recurrent pharyngitis or tonsillitis

Complications

Peritonsillar abscess may compromise the upper airway or spread into surrounding structures, including the masseter and pterygoid muscles, the lateral pharyngeal space, and the carotid sheath (see Figure 12). Spontaneous rupture of the abscess may cause asphyxiation or aspiration pneumonia.

Other complications include:

upper airway obstruction

aspiration pneumonia

lateral pharyngeal space infection

septic jugular thrombophlebitis (Lemierre’s syndrome; see Figure 14)

carotid sheath invasion and hemorrhage

necrotizing mediastinitis

Figure 14.

Contrast-enhenced axial CT of the neck in a young adult with jugular venous thrombosis associated with a lateral pharyngeal space infection secondary to a right peritonsillar abscess. The common carotid arteries (C) are normal but the right internal jugular vein (J) is enlarged with a dense or enhancing wall surrounding the more lucent intraluminal clot (arrow).

Prognosis

Most cases resolve without sequelae with early and appropriate treatment.

Recurrence may occur in 10-15% of cases (40% with history of recurrent tonsillitis).

Pathogenesis

Invasion by pathogenic bacteria (e.g., Group A Streptococcus and mixed aerobes and anaerobes) to cause pharyngitis and tonsillitis with progression to synergistic cellulites and abscess formation in the peritonsillar space

Rarely, peritonsillar abscess may also develop by hematogenous seeding of the salivary glands in the soft palate (Weber glands), which directly communicate with the tonsils.

Differential diagnosis

Acute epiglottitis (no trismus)

Retropharyngeal abscess (prominent neck stiffness but minimal or no trismus)

Lateral pharyngeal space infection due to spread from a parotid or submandibular space infection (bulging behind posterior tonsillar pillar rather than superior to the tonsil)

Prevention

DRG codes and expected length of stay

Expected length of hospital stay is 3-5 days.

WHAT'S THE EVIDENCE for specific management and treatment recommendations?

Use of steroids (methylprednisolone 2-3 mg/kg single dose IV) in peritonsillar abscess remains controversial. A single double-blind randomized clinical trial in 2004 showed significant improvement in symptoms (ability to swallow) and length of hospital stay in the steroid group compared to placebo. Confirmation with a larger study is needed before this can be routinely recommended.

Deep neck space infections

Deep neck space infections most commonly originate from a septic focus in mandibular molars, tonsils, parotid gland, deep cervical lymph nodes, paranasal sinuses, or mastoids. These infections occupy three important spaces embedded within different layers of the deep cervical fascia: the submandibular space (see Figure 15), the lateral pharyngeal (also known as parapharyngeal or pharyngomaxillary) space (see Figure 16), and the retropharyngeal space (see
Figure 17). Although rare in the post-antibiotic era, deep neck space infections are potentially life-threatening because of their proximity to the airway and vascular structures with potential spread into the carotid sheath, cavernous sinus, cranium, and the mediastinum (see Figure 3).

Laboratory investigation

Imaging studies

Lateral neck radiograph to assess airway and retropharyngeal soft tissues (normally about 5 mm deep, less than 1/3 the diameter of C4 vertebra; with retropharyngeal space infection, the pharynx or upper airway is displaced anteriorly by more than 1/2 the wide of C4 vertebra; see Figure 18).

Therapeutic considerations

Appropriate antibiotics in conjunction with surgical drainage of loculated infection are essential for successful outcome.Antimicrobial therapy

Choice of antimicrobial regimens is empirical, dependent on the primary source (e.g., odontogenic or oropharyngeal versus rhinogenic or otogenic), anticipated causative microorganisms, and immunity of the host.

Maximum doses should be administered to optimize tissue penetration and bactericidal activity.

Selection of subsequent antibiotics should be guided by culture data and susceptibility testing.

In immunocompromised hosts, broad-spectrum coverage for facultative gram-negative bacilli, as well as oral aerobes and anaerobes, should be included. In addition, patients with risk factors for methicillin-resistant Staphylococcus aureus (MRSA) infection should be treated empirically with vancomycin (15-20 mg/kg IV q 12h) or linezolid (600 mg IV q 12h). Risk factors for MRSA include history of intravenous drug abuse, comorbid disease (e.g., diabetes mellitus), and residence in a community or hospital with substantial incidence of MRSA (Table VI).

The primary pathology in deep neck space infection is a cellulitis that involves the connective tissues, fasciae, and muscles; surgical drainage should be implemented only if the cellulitic process has localized into a discrete abscess (as confirmed by CT or MRI).

Premature incision into an area of cellulitis area may actually worsen the situation by breaking down the natural barriers and hastening the spread of infection.

Complications

Carotid sheath involvement is a complication of lateral pharyngeal space infection with potential for carotid artery erosion or septic jugular thrombophlebitis (see Figure 12). Carotid artery mycotic aneurysm arises from arteritis due to contiguous inflammation, resulting eventually in formation of a false aneurysm, which may rupture. Characteristic clinical features include:

insidious onset with fever of unknown origin

recurrent “herald bleeds” from the nose, mouth, or ear

hematoma formation in the surrounding tissues

choice of antibiotics is the same as for lateral pharyngeal space infections from odontogenic or oropharyngeal sources (see
Table VI)

Septic jugular thrombophlebitis (Lemierre’s syndrome) is a complication of lateral pharyngeal space infection from odontogenic, parotid, or peritonsillar space infections (see
Figure 14) and should be suspected in patients with antecedent pharyngitis, septic pulmonary emboli, and persistent fever despite antibiotic therapy. Choice of antimicrobial regimens is the same as for lateral pharyngeal space infections from odontogenic or oropharyngeal sources.

Suppurative cavernous sinus thrombosis is a complication of sphenoid or ethmoid sinusitis and any septic foci of the face and head due to rich vascular supply and retrograde venous spread (see
Figure 19). Major clinical findings include:

The “danger” space lies posterior to the retropharyngeal space and extends from the base of the skull to the diaphragm via the entire length of the posterior mediastinum.

Sore throat or difficulty in swallowing or breathing may be the first indication of infection.

Diagnosis may be delayed because of trismus from primary sources of infection (e.g., odontogenic sepsis or peritonsillar abscess), which makes direct examination of the posterior pharyngeal wall difficult.

Reynolds, SC, Chow, AW. “Severe soft tissue infections of the head and neck: a primer for critical care physicians”. Lung. vol. 187. 2009. pp. 271-9. (This is a practical overview of the diagnosis and management of deep fascial space infections of the head and neck.)

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